Diesel exhaust (DE) is known to be one of the main causes of air pollution. Several studies have suggested that DE causes lung cancer, cardiovascular disease, abnormal reproductive function, and central nervous system damage as well as type I allergy in the airway. Type I allergy also plays a role in pathogenesis of endometriosis. In the present study, we examined the effect of exposure to DE on a rat model of endometriosis. Endometriosis was induced by autotransplantation of endometrium to the peritoneum in female Sprague-Dawley rats exposed to DE during prenatal and postnatal periods. Endometriotic lesions, normal peritoneum, and blood samples were obtained on days 4, 7, and 14 after autotransplantation. The extent of stromal proliferative lesions in the endometriosis model was greater in the rats of the DE exposure group than in those of the control group on day 14. Serum monocyte chemoattractant protein (MCP)-1 level was significantly higher in rats with endometriosis in the DE exposure group than in those in the control group on day 14. Results of this study suggest that DE exposure enhances the histologic and molecular pathology of endometriosis in rats.
-Previous studies have shown that prenatal and postnatal exposure to diesel exhaust (DE), which is known to be one of the main constituents of air pollution, enhances the persistence of endometriosis in a rat model. The aim of this study is to investigate the pathological changes induced by DE exposure in a rat model of endometriosis. Pregnant Sprague-Dawley rats were exposed to DE or clean air beginning on gestational day 2 and neonatal rats were persistently exposed to DE or clean air. Endometriosis was induced by autotransplantation of endometrium onto the peritoneum of eight-week-old female offspring. Endometriotic lesions were examined at 7 and 14 days post-transplantation. As a result, infiltration of activated mast cells remained in deeper area of peritoneal tissue around the endometriosis model compared to the control group at 14 days post-autotransplantation. In the DE exposure group, 14 days post-transplant, the remaining lesions contained fibroblasts and activated mast cells, which were surrounded by collagen fibers. The data showed that prenatal and postnatal DE exposure enhances the activation of mast cells and prolongs the persistence of collagen fibers in the induced rat model of endometriosis.
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